BACKGROUND: Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Recent data implicate disordered bone and mineral metabolism, including changes in serum levels of calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and fetuin A, as novel risk factors for arterial calcification. The potential role of calcitonin, another hormonal regulator of mineral and bone metabolism, has not been studied in detail. MATERIALS AND METHODS: We investigated the link between serum calcitonin and the total burden of coronary artery disease (CAD) using the validated Gensini score, in a cross-sectional study of 88 patients with estimated GFR (eGFR) between 46 and 87 ml/min/1.73 m² who underwent coronary angiography. We evaluated the associations between serum calcitonin, minerals (calcium, phosphate), calcium × phosphate product, and other factors that regulate mineral metabolism (intact PTH, 25-OH-vitamin D, FGF-23, and fetuin A) and the severity of CAD. RESULTS: The mean serum calcitonin was 11.5 ± 7.8 pg/ml. In univariate analysis, the Gensini CAD severity score correlated significantly with male gender, eGFR, and serum levels of 25-OH-vitamin D, iPTH, FGF-23, fetuin A, and calcitonin (R = 0.474, P = 0.001 for the latter). In multivariate analysis adjusted for calcium, phosphate, 25-OH-vitamin D, iPTH, FGF 23, fetuin A, and calcitonin, only calcitonin (β = 0.20; P = 0.03), FGF-23, fetuin A, and 25-OH-vitamin D emerged as independent predictors of Gensini score. In the second step, we adjusted for the presence of traditional risk factors, proteinuria, and GFR. After these adjustments, the FGF-23 and fetuin A remained statistically significant predictors of the Gensini score, while calcitonin did not. CONCLUSIONS: Our study suggests that, in addition to other well-known components of mineral metabolism, increased calcitonin levels are associated with greater severity of CAD. However, this relation was not independent of traditional and nontraditional cardiovascular risk factors. Longitudinal studies in larger populations including patients with more advanced CKD are needed.
BACKGROUND:Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Recent data implicate disordered bone and mineral metabolism, including changes in serum levels of calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and fetuin A, as novel risk factors for arterial calcification. The potential role of calcitonin, another hormonal regulator of mineral and bone metabolism, has not been studied in detail. MATERIALS AND METHODS: We investigated the link between serum calcitonin and the total burden of coronary artery disease (CAD) using the validated Gensini score, in a cross-sectional study of 88 patients with estimated GFR (eGFR) between 46 and 87 ml/min/1.73 m² who underwent coronary angiography. We evaluated the associations between serum calcitonin, minerals (calcium, phosphate), calcium × phosphate product, and other factors that regulate mineral metabolism (intact PTH, 25-OH-vitamin D, FGF-23, and fetuin A) and the severity of CAD. RESULTS: The mean serum calcitonin was 11.5 ± 7.8 pg/ml. In univariate analysis, the Gensini CAD severity score correlated significantly with male gender, eGFR, and serum levels of 25-OH-vitamin D, iPTH, FGF-23, fetuin A, and calcitonin (R = 0.474, P = 0.001 for the latter). In multivariate analysis adjusted for calcium, phosphate, 25-OH-vitamin D, iPTH, FGF 23, fetuin A, and calcitonin, only calcitonin (β = 0.20; P = 0.03), FGF-23, fetuin A, and 25-OH-vitamin D emerged as independent predictors of Gensini score. In the second step, we adjusted for the presence of traditional risk factors, proteinuria, and GFR. After these adjustments, the FGF-23 and fetuin A remained statistically significant predictors of the Gensini score, while calcitonin did not. CONCLUSIONS: Our study suggests that, in addition to other well-known components of mineral metabolism, increased calcitonin levels are associated with greater severity of CAD. However, this relation was not independent of traditional and nontraditional cardiovascular risk factors. Longitudinal studies in larger populations including patients with more advanced CKD are needed.
Authors: Giuseppe Mancia; Guy De Backer; Anna Dominiczak; Renata Cifkova; Robert Fagard; Giuseppe Germano; Guido Grassi; Anthony M Heagerty; Sverre E Kjeldsen; Stephane Laurent; Krzysztof Narkiewicz; Luis Ruilope; Andrzej Rynkiewicz; Roland E Schmieder; Harry Aj Struijker Boudier; Alberto Zanchetti Journal: J Hypertens Date: 2007-09 Impact factor: 4.844
Authors: P Niccoli; P Brunet; C Roubicek; F Roux; E Baudin; P J Lejeune; Y Berland; B Conte-Devolx Journal: Eur J Endocrinol Date: 1995-01 Impact factor: 6.664
Authors: M E Martínez; J L Miguel; P Gómez; R Selgas; M Salinas; M Gentil; F Mateos; J L Montero; L Sánchez Sicilia Journal: Clin Nephrol Date: 1983-05 Impact factor: 0.975
Authors: C Canavese; S Barolo; L Gurioli; A Cadario; M Portigliatti; G Isaia; A Thea; M Marangella; P Bongiorno; A Cavagnino; C Peona; R Boero; M D'Amicone; R Cardelli; P Rossi; G Piccoli Journal: Int J Artif Organs Date: 1998-08 Impact factor: 1.595
Authors: G H Daniels; L Hegedüs; S P Marso; M A Nauck; B Zinman; R M Bergenstal; J F E Mann; J Derving Karsbøl; A C Moses; J B Buse; R M Tuttle Journal: Diabetes Obes Metab Date: 2015-02-23 Impact factor: 6.577
Authors: Flávia Letícia Carvalho Gonçalves; Rosilene M Elias; Luciene M dos Reis; Fabiana G Graciolli; Fernando Godinho Zampieri; Rodrigo B Oliveira; Vanda Jorgetti; Rosa M A Moysés Journal: BMC Nephrol Date: 2014-12-02 Impact factor: 2.388